Despite the advances in modern health care, chronic wounds remain highly problematic. For the critically ill and those with mobility issues, missing just one routine repositioning could send them down a protracted path of intensive wound care therapies. Even our ambulatory patients develop non-healing ulcers from neuropathy and microvascular disease. For purposes of this discussion, the question of how the wound formed isn’t nearly as important as why it persists through all of our debridements, hyperbaric treatments, and cutting-edge antimicrobial dressings. Infectious Disease physicians typically become involved with these chronic wounds when patients present with signs of soft tissue infection – erythema, warmth, purulent drainage, and malodor. Most often, in these cases, I see my colleagues treat with one to two weeks of antibiotics and call it good. When wound-related sepsis and local findings of infection resolve, we like to believe that antibiotics have served their purpose. The problem is that many patients with chronic, deep wounds return in short order with recurrent signs of local infection, and we tend to rinse and repeat without breaking the cycle. After following hundreds of patients through this process, I have concluded that we fail to heal a lot of wounds because we miss a key underlying disease process – osteomyelitis. I can already hear the protests: “There’s no exposed bone in that wound!” “I biopsied the bone, and the path was negative!” All the same, osteomyelitis is primarily a clinical diagnosis. A positive path is great when you can get it, but we are frequently looking at a fingernail-sized piece of bone taken out of something as large as a sacrum. Osteomyelitis rarely affects the bone structure homogeneously – more often forming “islands” of infection in a sea of otherwise normal-appearing bone tissue. The potential for sampling error is great. I think there are also many cases where we do capture changes of osteomyelitis on path but don’t recognize them as such. The nonspecific necrotic/fibrotic changes seen in some bone biopsies, for example, may represent sequelae of chronic osteomyelitis where the organisms involved have destroyed the bone and moved on. However, if the pathology report doesn’t specifically say “osteomyelitis,” it doesn’t garner much attention. Sampling issues aside, biopsy is not our only means of making the diagnosis. The “probe-to-bone” test is still widely accepted as an indicator of probable osteomyelitis in diabetic foot wounds, so why not apply the same principle elsewhere on the body? If blindly finding a metatarsal at the end of a wound tunnel suggests osteomyelitis, shouldn’t we be more suspicious when we see a coccyx plainly protruding from a chronic decubitus ulcer? Bone tissue is quite susceptible to bacterial infection once stripped of its protective overlying soft tissue – so much so that I believe exposed bone equals infected bone. (Sorry, surgeon colleagues – you can’t declare that bone isn’t infected just because it looks intact.) We don’t even need a biopsy or imaging to prove it. In my experience, infected bone precludes durable formation of healthy soft tissue over the affected area, and this is what leads to the draining sinus that is pathognomonic of chronic osteomyelitis. Despite their diagnostic value, sinus tracts may not be recognized as such in the absence of visible bone. What do you suppose is causing the focus of deep tunneling in that chronic sacral wound, particularly when it won’t stop draining? Why do so many patients with recurrent wounds report that the breakdown started with a “pinhole” and drainage from the skin? I believe this is a clear indication of underlying bone infection – the product of bacteria reaching critical mass in the bone and dissecting out through the soft tissue. Unfortunately, osteomyelitis-related sinus tracts escape notice because they only rarely exude purulent drainage. Osteomyelitis may not provoke the kind of inflammation we associate with infection for several reasons. First, bone tissue gets comparatively little blood flow under the best of circumstances, so there’s already a bottleneck when it comes to mobilizing neutrophils. Second, osteomyelitis that has been present for a while can lead to necrosis of involved bone tissue, forming sequestrum. Between the sequestrum formation and the relatively low metabolic activity in normal bone, many infecting bacteria will enter a stationary phase to await better-growing conditions. To generate significant inflammation, you need a lot of immune cells reacting to a perceived threat, and this is ultimately why osteomyelitis gets missed – the confluence of poor blood blow and dormant invaders yields a lackluster immune response. I believe unrecognized osteomyelitis explains a lot of those cases in which a large pressure ulcer finally closes after months of regular visits to the wound care clinic, only to break down in spectacular fashion shortly after the patient is discharged. Doctors tend to blame the patient in that situation, suspecting that they stopped offloading or didn’t perform dressing changes correctly. While that’s certainly possible and probably explains some proportion of wound care failures, I have seen too many patients who were adamant that they continued doing their part only to have the wound break down anyway. Furthermore, many of these seemingly reliable patients went on to heal their wounds with prolonged courses of appropriate antibiotics based on wound culture results. I think it’s more likely that our efforts to reduce biofilm, debride necrotic tissue, and force more oxygen into the wound only transiently overcome the tissue-inhibiting effects of underlying osteomyelitis. As soon as we back off on the intensity of treatment, the wound returns with a vengeance. Of course, I can’t say that every non-healing wound is the result of underlying osteomyelitis, but I think it occurs often enough that it warrants a shift in our collective perspective. Rather than dismissing the possibility out of hand based on a single pathology study or the lack of erosive changes on X-ray, we need to raise our index of suspicion. After a few weeks of regular wound care, it might be time to stop thinking about the next best silver alginate hydrocolloid dressing and start thinking deeper. Clayton Foster is an infectious disease physician and founder, AirborneID. He can be reached on Facebook and Twitter @AirborneID_CO. Source
